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Inotropic Drugs

USMLE Step 1

DrugMOA & ADRs
Glycosides MOA MOA: inhibits the Na-K pump & thus as Na levels rise also inhibits the Na-Ca pump also allowing Ca to rise for aiding in increasing CO (used for severe LV systolic dysfx like CHF), derived from the foxglove plant
Glycosides ADRs (note enhanced by hypoK, alkalosis, hypoxia & hypothyroidism) ADRs: therapeutic index low, need regular monitoring serum levels, 1st indications of toxicity change in vision, arrhythmias & AV- due 2 hypokalemia (b careful w/ use of thiazides/loop diuretics), nausea, ab pain, fatigue, confusion, color misperception
Digitoxin MOA: glycoside that inhibits Na/K ATPase also allowing for increase in Na & Ca concs, ADRs: cant be used in those w/ liver probs since relies on liver for metabolism, long duration of action
Dobutamine MOA: beta-1 agonist that activate adenyl cyclase -> cAMP -> protein kinase -> phosphorylate Ca channels that increases Ca; ADRs: less tachy or peripheral side effects than isoproterenol or epi
Dopamine MOA: beta-1 agonist that activate adenyl cyclase -> cAMP -> protein kinase -> phosphorylate Ca channels that increases Ca, enhances renal flow thus used for tx of shock; ADRs: less tachy or peripheral side effects than isoproterenol or epi
Inamrinone MOA: Phosphodiesterase - that prevents the catabolism of cAMP in order to prolong action of protein kinase thus resulting in increase in intracellular Ca, *Note used to be called AMRINONE*; ADRs: thrombocytopenia
Milrinone MOA: Phosphodiesterase - that prevents the catabolism of cAMP in order to prolong action of protein kinase thus resulting in increase in intracellular Ca, doesnt affect platelets
Digoxin MOA: glycoside -Na/K ATPase decrease exchange levels in the Na/Ca thus result in higher levels of Ca, short duration of action; ADRs: low therapeutic index, excreted unchanged in urine
Created by: jerrica_08 on 2008-03-29




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